Muscle disease continues to represent a serious health problem. For example, Duchenne muscular dystrophy (DMD) is a severe sex-linked muscle wasting recessive disease affecting 1 in 3500 males at birth (Emery, 1993). It results from a mutation in the gene encoding the muscle protein dystrophin, a 427 kDa protein composed of 3685 amino acids (Hoffman et al., 1987). It is located just beneath the sarcolemma of skeletal myofibers and its absence in DMD patients causes sarcolemmal instability leading to frequent muscle fiber damage and repair (Blau et al., 1983). In dystrophic muscles, regeneration gradually fails and the normal cycle of degeneration-regeneration is tipped in favor of degeneration (Blau et al., 1983). This defective muscle repair due to myoblast senescence leads to death early in the third decade (Ohlendieck and Campbell, 1991). Delivery of normal dystrophin gene by the transplantation of non-dystrophic muscle derived precursor cells (i.e., myoblasts) results in the long-term restoration of this protein. Indeed the transplanted myoblasts fuse with the host fibers and introduce in them the normal dystrophin gene (Skuk and Tremblay, 2000). The success of myoblast transplantation is however reduced by the limited muscle regeneration in mdx mice and in DMD patients (Skuk and Tremblay, 2003). There thus remains a continued need for improved methods for the treatment of muscle disease.